Arbuscular mycorrhizal (AM) symbiosis in vascular plant roots is an ancient mutualistic interaction that evolved with land plants. More recently evolved root mutualisms have recruited components of the AM signalling pathway as identified with molecular approaches in model legume research. Earlier we reported that the reduced mycorrhizal colonisation (rmc) mutation of tomato mapped to chromosome 8. Here we report additional functional characterisation of the rmc mutation using genotype grafts and proteomic and transcriptomic analyses. Our results led to identification of the precise genome location of the Rmc locus from which we identified the mutation by sequencing. The rmc phenotype results from a deletion that disrupts five predicted gene sequences, one of which has close sequence match to the CYCLOPS/IPD3 gene identified in legumes as an essential intracellular regulator of both AM and rhizobial symbioses. Identification of two other genes not located at the rmc locus but with altered expression in the rmc genotype is also described. Possible roles of the other four disrupted genes in the deleted region are discussed. Our results support the identification of CYCLOPS/IPD3 in legumes and rice as a key gene required for AM symbiosis. The extensive characterisation of rmc in comparison with its 'parent' 76R, which has a normal mycorrhizal phenotype, has validated these lines as an important comparative model for glasshouse and field studies of AM and non-mycorrhizal plants with respect to plant competition and microbial interactions with vascular plant roots.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00572-013-0498-7DOI Listing

Publication Analysis

Top Keywords

rmc mutation
12
reduced mycorrhizal
8
mycorrhizal colonisation
8
rmc
8
colonisation rmc
8
mutation tomato
8
gene sequences
8
vascular plant
8
plant roots
8
characterisation rmc
8

Similar Publications

Spatial regulation of NSUN2-mediated tRNA m5C installation in cognitive function.

Nucleic Acids Res

December 2024

Department of Biochemistry and Biophysics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Enzyme-mediated modifications of tRNA, such as 5-methylcytosine (m5C) installed by nuclear-enriched NOP2/Sun RNA methyltransferase 2 (NSUN2), play a critical role in neuronal development and function. However, our understanding of these modifications' spatial installation and biological functions remains incomplete. In this study, we demonstrate that a nucleoplasm-localized G679R NSUN2 mutant, linked to intellectual disability, diminishes NSUN2-mediated tRNA m5C in human cell lines and Drosophila.

View Article and Find Full Text PDF
Article Synopsis
  • Genetic vascular disorders, particularly multisystemic smooth muscle dysfunction syndrome (MSMDS), result from mutations in the alpha actin isotype 2 gene and can lead to severe health issues such as stroke and early childhood death.
  • The research focused on correcting the common R179H mutation using a specially engineered CRISPR-Cas9 enzyme designed for high accuracy, decreasing unintended edits during the gene correction process.
  • By utilizing a murine model that mimics human MSMDS symptoms, the study demonstrated that delivering the customized editing tool significantly improved survival and health outcomes in affected mice, indicating potential for lasting treatments in humans.
View Article and Find Full Text PDF
Article Synopsis
  • * The only approved treatment, Rapamycin, offers limited benefits as lung function declines after stopping the drug, with LAM cancer stem-like cells displaying high levels of cancer-promoting protein synthesis.
  • * A new compound, RMC-5552, shows promise by effectively inhibiting LAM-associated cell growth and providing longer-lasting effects than Rapamycin, suggesting it could be a potential therapy for LAM and other conditions with mTORC1 hyperactivity.
View Article and Find Full Text PDF

Mutant selective drugs targeting the inactive, GDP-bound form of KRAS have been approved for use in lung cancer, but resistance develops rapidly. Here we use an inhibitor, (RMC-4998) that targets RAS in its active, GTP-bound form, to treat KRAS mutant lung cancer in various immune competent mouse models. RAS pathway reactivation after RMC-4998 treatment could be delayed using combined treatment with a SHP2 inhibitor, which not only impacts tumour cell RAS signalling but also remodels the tumour microenvironment to be less immunosuppressive.

View Article and Find Full Text PDF

RAS-ON inhibition overcomes clinical resistance to KRAS G12C-OFF covalent blockade.

Nat Commun

August 2024

Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino, Italy.

Selective KRAS inhibitors have been developed to covalently lock the oncogene in the inactive GDP-bound state. Two of these molecules, sotorasib and adagrasib, are approved for the treatment of adult patients with KRAS-mutated previously treated advanced non-small cell lung cancer. Drug treatment imposes selective pressures leading to the outgrowth of drug-resistant variants.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!